Uncertainty-guided cross learning via CNN and transformer for semi-supervised honeycomb lung lesion segmentation.

Objective. Deep learning networks such as convolutional neural networks (CNN) and Transformer have shown excellent performance on the task of medical image segmentation, however, the usual problem with medical images is the lack of large-scale, high-quality pixel-level annotations, which is a very time-consuming and laborious task, and its further leads to compromised the performance of medical image segmentation under limited annotation conditions.Approach. In this paper, we propose a new semi-supervised learning method, uncertainty-guided cross learning, which uses a limited number of annotated samples along with a large number of unlabeled images to train the network. Specifically, we use two networks with different learning paradigms, CNN and Transformer, for cross learning, and use the prediction of one of them as a pseudo label to supervise the other, so that they can learn from each other, fully extract the local and global features of the images, and combine explicit and implicit consistency regularization constraints with pseudo label methods. On the other hand, we use epistemic uncertainty as a guiding message to encourage the model to learn high-certainty pixel information in high-confidence regions, and minimize the impact of erroneous pseudo labels on the overall learning process to improve the performance of semi-supervised segmentation methods.Main results. We conducted honeycomb lung lesion segmentation experiments using a honeycomb lung CT image dataset, and designed several sets of comparison experiments and ablation experiments to validate the effectiveness of our method. The final experimental results show that the Dice coefficient of our proposed method reaches 88.49% on the test set, and our method achieves state-of-the-art performance in honeycomb lung lesion segmentation compared to other semi-supervised learning methods.Significance. Our proposed method can effectively improve the accuracy of segmentation of honeycomb lung lesions, which provides an important reference for physicians in the diagnosis and treatment of this disease.

Treatment with ginseng total saponins improves the neurorestoration of rat after traumatic brain injury.

ETHNOPHARMACOLOGICAL RELEVANCE: Ginseng, the root of Panax ginseng C.A. Meyer, is a traditional medicinal herb that has been widely used in Asia for the treatment of many diseases through its effects of reinforcing vitality, strengthening the bodily resistance to pathogenic factors, engendering body liquids and allaying thirst, relieving uneasiness of the body and mind and benefiting intelligence, reducing body weight and prolonging life. Ginsenosides are the most important biologically active substances in ginseng. Many reports have suggested that ginsenosides could exert prominent neuroprotective and neurotrophic effects, promote neural stem/progenitor cell (NSC) proliferation and promote neurite outgrowth and neuronal network formation. The present study aimed to investigate whether treatment with ginsenosides could facilitate NSC proliferation in the hippocampal formation after traumatic brain injury (TBI) and contribute to the recovery of neurological functions including learning and memory. MATERIALS AND METHODS: The modified Feeney׳s method was used to induce a TBI in rats. Ginseng total saponins (GTS) were treated intraperitoneally twice a day for 1 week after the TBI. The neurological functions, morphology of the hippocampus, expression of nerve growth-related factors and number of NSCs in the hippocampal formation ipsilateral to the trauma were determined. RESULTS: We determined 1) GTS (5-80 mg/kg) treatment after a TBI improved the recovery of neurological functions, including learning and memory, and reduced cell loss in the hippocampal area. The effects of GTS at 20, 40, 60, and 80 mg/kg were better than the effects of GTS at 5 and 10 mg/kg. 2) GTS treatment (20 mg/kg) after a TBI increased the expression of NGF, GDNF and NCAM, inhibited the expression of Nogo-A, Nogo-B, TN-C, and increased the number of BrdU/nestin positive NSCs in the hippocampal formation. CONCLUSIONS: GTS treatment in rats after a TBI alleviated the secondary brain injury and ameliorated the neurological functions with an effective dose limit of 5-80 mg/kg. GTS regulated the expression of nerve growth-related factors and improved the proliferation of neural stem/progenitor cells, which might facilitate neural regeneration and tissue repair, and might contribute to the recovery of neurological functions, including learning and memory. These effects of GTS might provide a foundation for the use of ginseng as a medicinal herb to enhance intelligence, reduce the aging process and prolong life in the traditional medicine.

L-serine treatment may improve neurorestoration of rats after permanent focal cerebral ischemia potentially through improvement of neurorepair.

The present study was conducted to clarify whether treatment with L-serine can improve the brain repair and neurorestoration of rats after permanent middle cerebral artery occlusion (pMCAO). After pMCAO, the neurological functions, brain lesion volume, and cortical injury were determined. GDNF, NGF, NCAM L1, tenascin-C, and Nogo-A levels were measured. Proliferation and differentiation of the neural stem cells (NSCs) and proliferation of the microvessels in the ischemic boundary zone of the cortex were evaluated. Treatment with L-serine (168 mg/kg body weight, i.p.) began 3 h after pMCAO and was repeated every 12 h for 7 days or until the end of the experiment. L-Serine treatment: 1) reduced the lesion volume and neuronal loss; 2) improved the recovery of neurological functions; 3) elevated the expression of nerve growth-related factors; and 4) facilitated the proliferation of endogenous NSCs and microvessels activated after pMCAO and increased the number of new-born neurons. 5) D-cycloserine, an inhibitor of serine hydroxymethyltransferase, blunted the effects of L-serine on NSC proliferation, differentiation, microvascular proliferation. In conclusions, L-serine treatment in pMCAO rats can reduce brain injury and facilitate neurorestoration which is partly associated with the improvement of proliferation of NSCs and microvessels, reconstruction of neurovascular units and resultant neurorepair. The effects of L-serine on endogenous NSC proliferation and microvascular proliferation are partly mediated by the action of L-serine as a substrate for the production of one-carbon groups used for purine and pyrimidine synthesis and modulation of the expression of some nerve growth-related factors.

Improvement in regional CBF by L-serine contributes to its neuroprotective effect in rats after focal cerebral ischemia.

To investigate the mechanisms underlying the neuroprotective effect of L-serine, permanent focal cerebral ischemia was induced by occlusion of the middle cerebral artery while monitoring cerebral blood flow (CBF). Rats were divided into control and L-serine-treated groups after middle cerebral artery occlusion. The neurological deficit score and brain infarct volume were assessed. Nissl staining was used to quantify the cortical injury. L-serine and D-serine levels in the ischemic cortex were analyzed with high performance liquid chromatography. We found that L-serine treatment: 1) reduced the neurological deficit score, infarct volume and cortical neuron loss in a dose-dependent manner; 2) improved CBF in the cortex, and this effect was inhibited in the presence of apamin plus charybdotoxin while the alleviation of both neurological deficit score and infarct volume was blocked; and 3) increased the amount of L-serine and D-serine in the cortex, and inhibition of the conversion of L-serine into D-serine by aminooxyacetic acid did not affect the reduction of neurological deficit score and infarct volume by L-serine. In conclusion, improvement in regional CBF by L-serine may contribute to its neuroprotective effect on the ischemic brain, potentially through vasodilation which is mediated by the small- and intermediate-conductance Ca(2+)-activated K(+) channels on the cerebral blood vessel endothelium.

Determinants of human population growth.

The 20th century has seen unprecedented growth of the human population on this planet. While at the beginning of the century the Earth had an estimated 1.6 billion inhabitants, this number grew to 6.1 billion by the end of the century, and further significant growth is a near certainty. This paper tries to summarize what factors lie behind this extraordinary expansion of the human population and what population growth we can expect for the future. It discusses the concept of demographic transition and the preconditions for a lasting secular fertility decline. Recent fertility declines in all parts of the world now make it likely that human population growth will come to an end over the course of this century, but in parts of the developing world significant population growth is still to be expected over the coming decades. The slowing of population growth through declining birth rates, together with still increasing life expectancy, will result in a strong ageing of population age structure. Finally, this paper presents a global level systematic analysis of the relationship between population density on the one hand, and growth and fertility rates on the other. This analysis indicates that in addition to the well-studied social and economic determinants, population density also presents a significant factor for the levels and trends of human birth rates.